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Translational Research
- Julie Sando, Ph.D., Professor of Research
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General anesthetics have been used clinically for over 100 years but their mechanism of action is not yet defined. The Myer-Overton correlation of anesthetic potency with oil-water partitioning has suggested interaction with both membrane lipids and with hydrophobic domains of proteins.
- Ganesan Kamatchi, Ph.D., Assistant Professor of Research
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Efforts in the laboratory are directed towards determining how anesthetic agents interfere with the enzyme protein kinase C and calcium channels. We have identified the sites of action of protein kinase C on various members of the calcium channels by comparing their amino acid sequence and also the evidence based on the published literature.
- Slobodan Todorovic, M.D., Ph.D., Associate Professor of Anesthesiology
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Our research interests involve studies of pharmacology and function of T-type (low-voltageactivated, LVA) calcium channels in sensory transmission. These channels have been identified in a variety of excitable and non-excitable cells.
- Vesna Todorovic, M.D., Ph.D., Associate Professor of Anesthesiology
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Broadly, my research interests focus on mechanisms by which anesthetic drugs interact with neurotransmitter systems in the central nervous system to produce both pharmacological and toxicological effects.
- Zhiyi Zuo, M.D., Ph.D., Associate Professor Anesthesiology & Neuroscience
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The research focuses in my laboratory are two: the regulation of glutamate transporters and neuroprotection.
- Manoj Patel, Ph.D., Assistant Professor of Research
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My research interests are divided into two main areas:
- Modulation of sodium channel gating by beta subunits and novel sodium channel blockers.
- The role of sodium channels in epilepsy.
- Lisa A. Palmer, Ph.D., Associate Professor of Research
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Our laboratory examines the regulation of the transcription factor hypoxia inducible factor-1 (HIF-1) by nitric oxide. We are currently examining (1) the mechanism by which NO induces the expression of HIF-1 and (2) the role of NO induced HIF-1 in the development of pulmonary hypertension.